It has been postulated since 1956 that the production of active oxygen species, or free radicals, pursuant to aerobic respiration, results in oxidative damage, which hastens aging and death in animals. See Beckman, K., et al., “The Free Radical Theory of Aging Matures,” Phys. Rev., 78: 547-581 (1998). Active oxygen species cause aging through various mechanisms, including directly damaging cellular DNA, see Cutler, R., “Antioxidants and aging”, Am. J. Clin. Nutr., 53: 373S-379S (1991), as well as lipids and proteins as well. See, Tylicki, L., et al. “Antioxidants: A Possible Role in Kidney Protection,” Kid. Bl. Press. Res., 26: 303-314 (2003). Free radicals, often produced in the mitochondria, where aerobic respiration occurs, damage mitochondrial DNA, proteins, and lipids. See, e.g., U.S. Patent App. Pub. No. US 2003/0060503.
It has also been postulated that active oxygen species may play a role in causing kidney disease. See, Ongajooth L., et al. “Role of Lipid Peroxidation, Trace Elements and Antioxidant Enzymes in Chronic Renal Disease Patients,” J. Med. Assc. Thai., 72:791-800 (1996). Several mechanisms have been proposed to account for this increase in renal failure (see, e.g., Hasselwander, et al. “Oxidative Stress in Chronic Renal Failure,” Free Rad. Res. 29:1-11 (1998); Shah, S., “The Role of Reactive Oxygen Metabolites in Glomerular Disease,” Annu. Rev. Physiol., 57:245-62 (1995)), but scientific studies to date are inconclusive regarding whether antioxidant treatment is beneficial to those with kidney disease. Some studies indicate that there is a role for various antioxidant supplementation in the protection against kidney disease. See, e.g., Kedziora-Komatowska, “Effect of Vitamin E and Vitamin C Supplementation on Antioxidative State and Renal Glomerular Basement Membrane Thickness in Diabetic Kidney”, Nephron Exp. Nephrol., 95:e134-e143 (2003). Other studies note the potential pro-oxidant properties of antioxidant supplements, concluding that there is not yet enough experimental evidence to recommend antioxidant supplements to alleviate kidney disease. See, e.g., Tylicki, L., et al.
In addition to the improvement of kidney function caused by supplementation of an animal's diet with antioxidants, kidney function may also benefit from the avoidance of mineral excess. Byproducts of protein digestion and phosphorus are among the primary toxins that must be removed from the blood stream by the kidneys. Thus, by decreasing protein and/or phosphorus consumption in an animal's diet, less stress is placed upon kidney function, improving kidney health. In short, lowering the dietary intake of protein and/or phosphorus is beneficial to improving kidney function and/or lessening the progression of renal disease. See, e.g. U.S. Pat. No. 6,306,442.
Despite years of studies and developments relating to renal function and kidney disease, there continues to be a need for compositions and methods that aid in improving kidney function.